Membranous nephropathy: new pathogenic mechanisms and their clinical implications

Elion Hoxha; Linda Reinhard; Rolf A K Stahl

doi:10.1038/s41581-022-00564-1

Membranous nephropathy: new pathogenic mechanisms and their clinical implications

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Membranous nephropathy: new pathogenic mechanisms and their clinical implications. / Hoxha, Elion; Reinhard, Linda; Stahl, Rolf A K.

In: NAT REV NEPHROL, Vol. 18, No. 7, 07.2022, p. 466-478.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Hoxha, E, Reinhard, L & Stahl, RAK 2022, 'Membranous nephropathy: new pathogenic mechanisms and their clinical implications', NAT REV NEPHROL, vol. 18, no. 7, pp. 466-478. https://doi.org/10.1038/s41581-022-00564-1

APA

Hoxha, E., Reinhard, L., & Stahl, R. A. K. (2022). Membranous nephropathy: new pathogenic mechanisms and their clinical implications. NAT REV NEPHROL, 18(7), 466-478. https://doi.org/10.1038/s41581-022-00564-1

Vancouver

Hoxha E, Reinhard L, Stahl RAK. Membranous nephropathy: new pathogenic mechanisms and their clinical implications. NAT REV NEPHROL. 2022 Jul;18(7):466-478. https://doi.org/10.1038/s41581-022-00564-1

Bibtex

@article{f40336acb3f34f9ba45f3ecd5f0d21be,

title = "Membranous nephropathy: new pathogenic mechanisms and their clinical implications",

abstract = "Membranous nephropathy (MN) is characterized histomorphologically by the presence of immune deposits in the subepithelial space of the glomerular filtration barrier; its clinical hallmarks are nephrotic range proteinuria with oedema. In patients with primary MN, autoimmunity is driven by circulating autoantibodies that bind to one or more antigens on the surface of glomerular podocytes. Compared with other autoimmune kidney diseases, the understanding of the pathogenesis of MN has substantially improved in the past decade, thanks to the discovery of pathogenic circulating autoantibodies against phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type 1 domain-containing protein 7A (THSD7A). The subsequent identification of more proteins associated with MN, some of which are also endogenous podocyte antigens, might further advance the clinical characterization of MN, including its diagnosis, treatment and prognosis. Insights from studies in patients with MN, combined with the development of novel in vivo and in vitro experimental models, have potential to improve the management of patients with MN. Characterizing the interaction between autoimmunity and local glomerular lesions provides an opportunity to develop more specific, pathogenesis-based treatments.",

author = "Elion Hoxha and Linda Reinhard and Stahl, {Rolf A K}",

note = "{\textcopyright} 2022. Springer Nature Limited.",

year = "2022",

month = jul,

doi = "10.1038/s41581-022-00564-1",

language = "English",

volume = "18",

pages = "466--478",

journal = "NAT REV NEPHROL",

issn = "1759-5061",

publisher = "NATURE PUBLISHING GROUP",

number = "7",

}

RIS

TY - JOUR

T1 - Membranous nephropathy: new pathogenic mechanisms and their clinical implications

AU - Hoxha, Elion

AU - Reinhard, Linda

AU - Stahl, Rolf A K

PY - 2022/7

Y1 - 2022/7

N2 - Membranous nephropathy (MN) is characterized histomorphologically by the presence of immune deposits in the subepithelial space of the glomerular filtration barrier; its clinical hallmarks are nephrotic range proteinuria with oedema. In patients with primary MN, autoimmunity is driven by circulating autoantibodies that bind to one or more antigens on the surface of glomerular podocytes. Compared with other autoimmune kidney diseases, the understanding of the pathogenesis of MN has substantially improved in the past decade, thanks to the discovery of pathogenic circulating autoantibodies against phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type 1 domain-containing protein 7A (THSD7A). The subsequent identification of more proteins associated with MN, some of which are also endogenous podocyte antigens, might further advance the clinical characterization of MN, including its diagnosis, treatment and prognosis. Insights from studies in patients with MN, combined with the development of novel in vivo and in vitro experimental models, have potential to improve the management of patients with MN. Characterizing the interaction between autoimmunity and local glomerular lesions provides an opportunity to develop more specific, pathogenesis-based treatments.

AB - Membranous nephropathy (MN) is characterized histomorphologically by the presence of immune deposits in the subepithelial space of the glomerular filtration barrier; its clinical hallmarks are nephrotic range proteinuria with oedema. In patients with primary MN, autoimmunity is driven by circulating autoantibodies that bind to one or more antigens on the surface of glomerular podocytes. Compared with other autoimmune kidney diseases, the understanding of the pathogenesis of MN has substantially improved in the past decade, thanks to the discovery of pathogenic circulating autoantibodies against phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type 1 domain-containing protein 7A (THSD7A). The subsequent identification of more proteins associated with MN, some of which are also endogenous podocyte antigens, might further advance the clinical characterization of MN, including its diagnosis, treatment and prognosis. Insights from studies in patients with MN, combined with the development of novel in vivo and in vitro experimental models, have potential to improve the management of patients with MN. Characterizing the interaction between autoimmunity and local glomerular lesions provides an opportunity to develop more specific, pathogenesis-based treatments.

U2 - 10.1038/s41581-022-00564-1

DO - 10.1038/s41581-022-00564-1

M3 - SCORING: Review article

C2 - 35484394

VL - 18

SP - 466

EP - 478

JO - NAT REV NEPHROL

JF - NAT REV NEPHROL

SN - 1759-5061

IS - 7

ER -